Kelemen K, Marko R, Kecskemeti V
Pol J Pharmacol Pharm. 1985 May-Jun;37(3):421-7.
Dopamine increased the slow inward current in the cardiac preparation after blocking (with tetrodotoxin) or eliminating (with Na+-free perfusion) of the "fast Na+ channel". Dopamine was, however, ineffective, if the "slow channel" was blocked (by MnCl2 or D-600) or eliminated (by Ca2+ free perfusion). This adrenaline-like effect of dopamine was prevented by beta-adrenergic blockade (pindolol) and was not modified by previous depletion of tissue catecholamine stores (pretreatment with reserpine). Our data suggest that dopamine affects cardiac electrogenesis through beta-adrenergic receptors and any dopamine-induced noradrenaline release may be only of secondary importance beside this direct agonistic effect.
在（用河豚毒素）阻断或（用无钠灌注）消除“快钠通道”后，多巴胺增加了心脏标本中的缓慢内向电流。然而，如果“慢通道”被（氯化锰或D - 600）阻断或（用无钙灌注）消除，多巴胺则无效。多巴胺的这种类似肾上腺素的作用可被β - 肾上腺素能阻断剂（吲哚洛尔）阻止，并且不受先前组织儿茶酚胺储备耗竭（利血平预处理）的影响。我们的数据表明，多巴胺通过β - 肾上腺素能受体影响心脏电活动，并且任何多巴胺诱导的去甲肾上腺素释放与此直接激动作用相比可能仅具有次要意义。
